Contact Dermatitis

Quick Reference

Critical Alerts

• Type IV hypersensitivity reaction: Delayed onset 24-72 hours, T-cell mediated
• Differentiate ICD from ACD: 80% irritant (immediate), 20% allergic (delayed)
• Distinguish from cellulitis: Pruritic (not tender), well-demarcated, geometric patterns
• Patch testing is gold standard: Identifies specific allergens in ACD
• Occupational disease: Leading cause of occupational skin disease (> 40% of cases)
• Chronic hand eczema: Most common anatomical site, significant disability
• Systemic steroids require taper: 2-3 weeks to prevent rebound dermatitis
• Secondary infection risk: Monitor for impetiginization and cellulitis

Irritant vs Allergic Contact Dermatitis

Common Contact Allergens by Category

Emergency Treatments

---

Definition

Overview

Contact dermatitis is an inflammatory eczematous skin reaction caused by direct contact with external substances. It represents a major public health burden, accounting for over 40% of all occupational skin diseases and affecting approximately 15-20% of the general population. Contact dermatitis is classified into two principal types based on pathophysiology: irritant contact dermatitis (ICD), caused by direct cytotoxic damage to keratinocytes without immunological sensitization, and allergic contact dermatitis (ACD), a T-cell-mediated delayed-type hypersensitivity reaction requiring prior sensitization. [1,2,3]

Classification

By Mechanism:

By Clinical Pattern:

Epidemiology

• Prevalence: 15-20% lifetime prevalence in general population [4]
• Incidence: 5.7 per 1,000 person-years
• ICD vs ACD ratio: 80% ICD, 20% ACD [1]
• Sex distribution: Females > males (2:1) due to higher exposure to cosmetics and jewelry
• Age: Can occur at any age; ACD prevalence increases with age and cumulative exposure
• Occupational: Leading cause of occupational skin disease
  • Accounts for 40-50% of all occupational diseases [5]
  • 70% affects hands (occupational hand dermatitis)
  • "High-risk occupations: healthcare workers, hairdressers, construction workers, food handlers, metalworkers, cleaners"
• Geographic variation: Nickel allergy higher in Europe (piercing practices), chromate allergy higher in construction workers
• Economic burden: Significant costs from lost work time, disability claims, healthcare utilization

Etiology

Irritant Contact Dermatitis Causes:

Allergic Contact Dermatitis Allergens:

---

Pathophysiology

Irritant Contact Dermatitis: Non-Immunological Pathway

Barrier Disruption and Innate Immunity:

Irritant contact dermatitis results from direct chemical or physical damage to the skin barrier without requiring prior sensitization or adaptive immune memory. The pathophysiology involves multiple overlapping mechanisms [6,7]:

1. Stratum Corneum Disruption:

   • Lipid extraction and protein denaturation
   • Disruption of tight junctions between keratinocytes
   • Increased transepidermal water loss (TEWL)
   • Impaired barrier function allows deeper penetration of irritants

2. Keratinocyte Activation:

   • Direct cytotoxic damage triggers keratinocyte stress response
   • Release of damage-associated molecular patterns (DAMPs)
   • Activation of pattern recognition receptors (PRRs)
   • Production of pro-inflammatory cytokines: IL-1α, IL-1β, TNF-α, IL-6, IL-8

3. Innate Immune Activation:

   • Cytokine cascade recruits innate immune cells
   • Neutrophil infiltration (early phase)
   • Macrophage activation
   • Natural killer (NK) cell recruitment
   • NO adaptive immune response or immunological memory

4. Cumulative Insult Dermatitis:

   • Repeated subclinical exposures prevent barrier recovery
   • Progressive barrier dysfunction
   • Chronic inflammation
   • Common in occupational settings ("wet work")

Clinical Correlate: ICD severity correlates with irritant concentration, exposure duration, and baseline barrier integrity. Individuals with filaggrin mutations or atopic dermatitis have increased susceptibility due to impaired barrier function. [8]

Allergic Contact Dermatitis: Type IV Hypersensitivity

Allergic contact dermatitis is a classic example of Type IV delayed-type hypersensitivity mediated by hapten-specific T lymphocytes. The process occurs in two distinct immunological phases [9,10,11]:

Phase 1: Sensitization (Afferent Phase)

Duration: 10-14 days (first exposure)

1. Hapten Penetration and Protein Binding:

   • Most contact allergens are small lipophilic molecules (less than 500 Da) called haptens
   • Haptens are incomplete antigens that cannot elicit immune response alone
   • Penetrate stratum corneum and covalently bind to self-proteins (carrier proteins)
   • Formation of hapten-protein conjugates creates immunogenic complexes
   • Pro-haptens: activated by skin metabolism (e.g., fragrance terpenes)
   • Pre-haptens: require oxidation (e.g., linalool in fragrances)

2. Innate Immune Activation and "Danger Signals":

   • Keratinocytes respond to hapten-induced stress
   • Release of IL-1β, TNF-α, and GM-CSF
   • These cytokines activate resident Langerhans cells (LCs) and dermal dendritic cells (DCs)
   • Expression of co-stimulatory molecules (CD80, CD86) on DCs
   • Without concurrent "danger signals," haptens may induce tolerance rather than sensitization

3. Dendritic Cell Maturation and Migration:

   • Langerhans cells in epidermis capture hapten-protein conjugates
   • Maturation process: upregulation of MHC class I and II, CD80, CD86, CCR7
   • Migration via afferent lymphatics to regional lymph nodes (24-48 hours)
   • Driven by chemokine gradients (CCL19, CCL21)

4. T Cell Priming in Lymph Nodes:

   • DCs present processed hapten-peptide complexes on MHC molecules
   • MHC Class I pathway: Presentation to CD8+ T cells (cytotoxic effectors)
   • MHC Class II pathway: Presentation to CD4+ T helper cells
   • CD1 molecules: Non-classical presentation pathway for lipophilic haptens
   • T cell activation requires three signals:
     • Signal 1: TCR recognition of MHC-peptide complex
     • Signal 2: Co-stimulation (CD28-CD80/86)
     • Signal 3: Cytokine milieu (IL-12, IL-18)
   • Clonal expansion of hapten-specific T cells (10³-10⁵ fold expansion)
   • Differentiation into effector and memory T cells

5. Effector T Cell Phenotypes:

   • CD8+ Type 1 T cells: Primary effectors in most ACD
     • Produce IFN-γ (Type IVc reaction)
     • Cytotoxic mechanisms: perforin, granzyme B, Fas-FasL
   • CD4+ Th1 cells: Amplify inflammation (Type IVa)
     • Produce IFN-γ, TNF-α, IL-2
     • Activate macrophages
   • CD4+ Th2 cells: In some allergens (Type IVb)
     • Produce IL-4, IL-5, IL-13
     • Eosinophil recruitment
   • Th17 cells: Neutrophilic inflammation (Type IVd)
     • Produce IL-17, IL-22
     • Seen in pustular reactions

6. Memory Phase:

   • Generation of tissue-resident memory T cells (TRM)
   • TRM persist in skin at site of sensitization
   • Express CD69 (retention marker) and CD103 (epithelial adhesion)
   • Rapid recall response upon re-exposure [12]

Phase 2: Elicitation (Efferent Phase)

Duration: 24-72 hours (upon re-exposure)

1. Re-exposure and Antigen Recognition:

   • Hapten re-enters skin and binds proteins
   • Presented by local keratinocytes (MHC I), Langerhans cells, dermal DCs
   • Recognition by circulating memory T cells and skin-resident TRM

2. Rapid T Cell Activation:

   • TRM provide immediate local response (within hours)
   • Circulating memory T cells recruited from blood
   • Expression of cutaneous lymphocyte antigen (CLA) for skin homing
   • Chemokine receptors (CCR4, CCR10) guide migration

3. Effector Mechanisms:

   Cytotoxicity (CD8+ T cells):

   • Direct killing of hapten-bearing keratinocytes
   • Perforin/granzyme-mediated apoptosis
   • Fas-FasL pathway activation
   • Results in spongiosis and vesicle formation

   Cytokine-Mediated Inflammation (CD4+ and CD8+):

   • IFN-γ: Keratinocyte activation, adhesion molecule upregulation (ICAM-1, VCAM-1)
   • TNF-α: Endothelial activation, leukocyte recruitment
   • IL-2: T cell proliferation
   • IL-17: Neutrophil recruitment (in pustular variants)

4. Amplification Cascade:

   • Keratinocyte production of IL-1, IL-6, IL-8, TNF-α
   • Chemokine production (CXCL9, CXCL10, CCL20) recruits more T cells
   • Endothelial adhesion molecule expression (E-selectin, ICAM-1)
   • Leukocyte infiltration: T cells, macrophages, eosinophils

5. Clinical Manifestation:

   • Spongiosis: Intercellular edema in epidermis from cytokine-induced fluid accumulation
   • Vesicle formation: Coalescence of spongiotic foci
   • Acanthosis: Epidermal thickening from keratinocyte proliferation
   • Dermal inflammation: Perivascular lymphocytic infiltrate
   • Symptoms: Pruritus (from histamine, tryptase, neuropeptides), erythema, vesiculation

6. Resolution and Regulatory Mechanisms:

   • Regulatory T cells (Tregs): CD4+CD25+FoxP3+ suppress effector T cells
   • IL-10 production by Tregs inhibits DC activation
   • Apoptosis of activated effector T cells
   • Barrier repair and inflammation resolution
   • Persistence of TRM maintains capacity for flare-ups [13]

Skin Barrier Role in Contact Dermatitis

The skin barrier is both target and modulator of contact dermatitis [14]:

• Barrier dysfunction increases penetration: Filaggrin mutations, atopic dermatitis, irritant pre-exposure
• Barrier disruption provides danger signals: Required for sensitization in ACD
• Occupational exposure: Repeated barrier disruption increases both ICD and ACD risk
• Preventive strategies: Barrier protection (gloves, emollients) reduces incidence

Genetic Susceptibility

• Filaggrin mutations: Increased risk of hand eczema and occupational dermatitis
• HLA associations: Certain HLA alleles linked to specific allergen sensitivities
  • "HLA-DR4: Nickel allergy"
  • "HLA-DRB1*0101: Chromate allergy"
• Metabolic enzyme polymorphisms: Affect pro-hapten activation

---

Clinical Presentation

Symptoms

History: Key Questions

Exposure History:

• "What products do you use on your skin?" (soaps, lotions, cosmetics)
• "Have you started any new products recently?" (temporal relationship)
• "What is your occupation?" (occupational exposures)
• "Do you work with chemicals, water, or wear gloves frequently?" (occupational ICD/ACD)
• "Do you wear jewelry?" (nickel, cobalt)
• "Have you been outdoors in wooded areas?" (poison ivy/oak/sumac)
• "Do you use hair dyes or cosmetics?" (PPD, fragrances, preservatives)

Temporal Pattern:

• "When did the rash start in relation to exposure?" (immediate vs. delayed)
• "Does it improve when away from work or on vacation?" (occupational)
• "Does it recur in the same location?" (suggests local contactant)
• "Have you had similar episodes before?" (recurrent ACD)

Distribution Pattern:

• "Where did it start and how has it spread?"
• "Does it correspond to areas of contact with specific items?"

Previous Medical History:

• Personal or family history of atopy (atopic dermatitis, asthma, allergic rhinitis)
• Previous episodes of contact dermatitis
• Known contact allergies (from prior patch testing)
• Occupational skin disease claims

Physical Examination

Distribution Patterns and Diagnostic Clues

Morphology by Phase

Acute Contact Dermatitis:

• Bright erythema
• Edema (may be pronounced on eyelids, genitals)
• Vesicles and bullae (more common in ACD)
• Weeping and oozing from ruptured vesicles
• Well-demarcated borders
• Linear configuration (poison ivy)

Subacute Contact Dermatitis:

• Erythema (less intense)
• Scaling
• Crusting
• Mild lichenification

Chronic Contact Dermatitis:

• Lichenification (thickened, leathery skin)
• Hyperkeratosis
• Fissuring (painful cracks, especially hands)
• Hyperpigmentation or hypopigmentation
• Less distinct borders
• Chronic hand eczema appearance

Specific Clinical Syndromes

Occupational Hand Dermatitis

• Most common presentation of occupational contact dermatitis (70% of cases)
• Affects healthcare workers, food handlers, hairdressers, cleaners, metalworkers
• ICD more common than ACD in occupational setting (but often coexist)
• Chronic, relapsing course
• Significant functional impairment and disability
• Fissuring on palms and fingertips particularly painful

Poison Ivy/Oak/Sumac Dermatitis (Toxicodendron)

• Caused by urushiol oleoresin
• Highly allergenic; up to 50-75% of population can sensitize
• Classic linear streaks: From brushing against plant or scratching
• Vesicles and bullae common
• Face, hands, arms most commonly affected
• Urushiol persists on clothing, tools, pet fur → can cause dermatitis without direct plant contact
• "Black dot sign": Oxidized urushiol appears as black dots on skin
• Severe reactions may require systemic corticosteroids for 2-3 weeks

Nickel Dermatitis

• Most common contact allergen worldwide (15-30% prevalence in patch-tested populations)
• More common in females (jewelry, piercings)
• Typical sites: Earlobes (earrings), wrists (watches), periumbilical (belt buckles), hands (coins, keys)
• "Dimple sign": Dermatitis precisely at site of metal contact
• Cross-reactivity with cobalt and chromate common
• Systemically absorbed nickel can cause systemic contact dermatitis (pompholyx, dyshidrotic eczema)

Fragrance Dermatitis

• Fragrance mix I and II among top allergens
• Fragrances ubiquitous: personal care products, household cleaners, air fresheners
• Balsam of Peru (Myroxylon pereirae) common; cross-reacts with fragrances, spices, citrus
• Often facial involvement (cosmetics)
• Difficult to avoid due to ubiquitous exposure
• "Fragrance-free" vs. "unscented" labeling important

Preservative Dermatitis

• Methylisothiazolinone (MI) epidemic in recent years due to increased cosmetic use
• MCI/MI (Kathon CG) also common
• Formaldehyde and formaldehyde-releasers (quaternium-15, DMDM hydantoin, imidazolidinyl urea)
• Widespread use in cosmetics, household products, industrial applications

Rubber/Glove Dermatitis

• Thiuram, carba mix, mercaptobenzothiazole (rubber accelerators)
• Occupational: healthcare workers, food handlers, hairdressers
• Often hand dermatitis mimicking ICD from wet work
• Type IV (ACD to accelerators) vs. Type I (IgE-mediated latex allergy)
• Patch testing distinguishes ACD from ICD or latex allergy

Cosmetic Dermatitis

• Fragrances, preservatives, PPD (hair dye), propylene glycol, cocamidopropyl betaine
• Facial involvement common
• Eyelid dermatitis from nail polish (indirect transfer)
• Hair dye (PPD) can cause severe facial and scalp swelling

---

Red Flags

Severe Reactions Requiring Urgent Intervention

Secondary Infection

Atypical Features Suggesting Alternative Diagnosis

---

Differential Diagnosis

Eczematous Dermatoses

Infectious Causes

Other Inflammatory Dermatoses

Immunobullous Disorders (if bullous)

---

Diagnostic Approach

Clinical Diagnosis

Contact dermatitis is primarily a clinical diagnosis based on:

1. History: Exposure to potential irritant or allergen
2. Temporal relationship: Onset in relation to exposure; improvement with avoidance
3. Distribution: Corresponds to contact pattern
4. Morphology: Eczematous dermatitis (acute, subacute, or chronic)

Key Principle: The combination of exposure history + characteristic distribution + eczematous morphology establishes the diagnosis of contact dermatitis.

Patch Testing: Gold Standard for ACD

Patch testing is the reference standard for identifying specific allergens in allergic contact dermatitis. [15,16]

Indications for Patch Testing

• Suspected allergic contact dermatitis (especially chronic or recurrent)
• Chronic hand dermatitis (high yield for identifying allergens)
• Occupational dermatitis
• Facial dermatitis (cosmetics, fragrances)
• Dermatitis unresponsive to treatment
• Recurrent dermatitis after apparent resolution
• Uncertain diagnosis (distinguish ACD from other eczematous dermatoses)

Patch Testing Procedure

Preparation:

• Discontinue systemic corticosteroids ≥2 weeks, topical corticosteroids to back ≥1 week (to avoid false negatives)
• Avoid antihistamines if possible (do not affect patch test but may reduce itch)
• Test during quiescent phase (active dermatitis can cause false positives)
• Back should be free of active dermatitis

Standard Panels:

• North American Standard Series: 80+ allergens (most common in North America)
• European Standard Series: Slightly different composition
• Specialized panels: Cosmetics, fragrances, metals, rubber, acrylates, topical medications, dental, occupational

Application:

• Allergens applied in Finn chambers or similar devices
• Applied to upper back (standard location)
• Kept in place for 48 hours (intact, avoid sweating/bathing)

Reading Schedule:

• First reading: 48 hours (at removal)
• Second reading: 96 hours (day 4) or 72-120 hours
• Some allergens require late readings (day 7) due to delayed reactions (e.g., corticosteroids, neomycin)

Interpretation (ICDRG Scale):

Relevance Assessment:

Positive patch test must be correlated with clinical history to determine relevance:

• Current relevance: Allergen explains current dermatitis
• Past relevance: Explained past episode but not current
• Possible relevance: Uncertain relationship
• Not relevant: Positive test but no clinical correlation

Only relevant positive reactions guide avoidance recommendations.

Pitfalls in Patch Testing

• False negatives: Corticosteroid use, insufficient allergen concentration, testing during flare
• False positives: Irritant reactions, "angry back" (generalized hyperreactivity), tape reactions
• Delayed reactions: Some allergens (corticosteroids, neomycin) require late readings
• Active sensitization: Patch testing can rarely induce new sensitization (especially strong sensitizers)

Laboratory/Imaging

Generally Not Required: Contact dermatitis is a clinical and patch test diagnosis. Laboratory tests are not routinely indicated unless considering alternative diagnoses or complications.

Specific Tests (When Indicated):

Histopathology (if biopsy performed):

• Acute: Spongiosis (intercellular edema), vesicle formation, perivascular lymphocytic infiltrate
• Chronic: Acanthosis (epidermal thickening), hyperkeratosis, lichenification, less spongiosis
• ACD vs. ICD: Histology generally cannot reliably distinguish; diagnosis is clinical

---

Treatment

General Principles

1. Identify and remove offending agent: Most critical step; resolution impossible with continued exposure
2. Restore skin barrier: Emollients, avoid irritants, gentle cleansers
3. Reduce inflammation: Topical corticosteroids (first-line), systemic if severe
4. Symptomatic relief: Antihistamines for pruritus, cool compresses
5. Treat secondary infection: Antibiotics if impetiginized or cellulitis
6. Prevention: Patient education, avoidance strategies, occupational modifications, protective equipment

Remove Offending Agent

Immediate Actions:

• Wash skin: Soap and water immediately after suspected contact (especially plant exposure)
  • Urushiol can be removed if washed within 10-15 minutes
  • After 30 minutes, most has penetrated skin
• Remove contaminated clothing: Wash in hot water with detergent
• Clean objects that may carry allergen: Tools, pet fur, gardening equipment (urushiol persists)
• Identify and avoid re-exposure: Based on history or patch testing results

Avoidance Strategies (after allergen identification):

• Nickel: Avoid costume jewelry, use hypoallergenic metals (titanium, surgical steel, gold > 18K), coat metal objects with clear nail polish
• Fragrances: Use fragrance-free products; "unscented" may contain masking fragrances
• Preservatives (MI/MCI): Read product labels, use preservative-free alternatives
• Rubber: Use vinyl or nitrile gloves instead of latex/rubber
• Cosmetics: Hypoallergenic, fragrance-free, preservative-free products
• Occupational: Barrier protection (gloves), job modification, industrial hygiene measures

Topical Corticosteroids

Topical corticosteroids are first-line treatment for contact dermatitis. Potency should be matched to site and severity. [17]

Potency Classification

Application Guidelines

• Frequency: Typically BID (twice daily) until improvement, then taper
• Duration: 2-4 weeks for most cases; avoid prolonged super-high potency (max 2 weeks)
• Amount: Fingertip unit (FTU) = 0.5 grams; one FTU covers two adult palms
• Vehicle:
  • "Ointments: More occlusive, more potent, better for dry/chronic/lichenified dermatitis"
  • "Creams: Less greasy, better for acute/weeping dermatitis"
  • "Lotions/solutions: For scalp, hairy areas"
  • "Gels: For hairy areas"
• Taper: Step down potency or reduce frequency as improvement occurs

Adverse Effects

• Local: Skin atrophy, striae, telangiectasia, acne, rosacea, perioral dermatitis (especially face)
• Systemic (rare with topical use): HPA axis suppression with prolonged super-high potency over large BSA
• Steroid allergy: Paradoxical—contact allergy to topical corticosteroid (patch test to corticosteroid panel if suspected)

Systemic Corticosteroids

Indicated for severe, widespread, or bullous contact dermatitis. [18]

Indications

• Moderate-severe poison ivy/oak/sumac (widespread, facial involvement)
• > 10-20% BSA involvement
• Severe symptoms (intense pruritus, pain, functional impairment)
• Bullous reactions
• Facial/periorbital involvement causing significant swelling
• Failed topical therapy

Regimens

Prednisone (most common):

Critical Point: Short courses (less than 10-14 days) of systemic corticosteroids are associated with high rates of rebound dermatitis. A 2-3 week taper is required for severe ACD, especially poison ivy/oak/sumac. [18]

Methylprednisolone dose pack (6-day taper): Generally NOT recommended for contact dermatitis due to insufficient duration and high rebound rate.

IM corticosteroids:

• Triamcinolone acetonide 40-80 mg IM (single dose)
• May be used for non-compliant patients
• Longer duration but cannot adjust dose if side effects; less preferred

Contraindications/Precautions

• Active infection (relative)
• Diabetes (monitor glucose)
• Hypertension
• Peptic ulcer disease
• Psychiatric disease
• Pregnancy (Category C; use if benefits outweigh risks)

Topical Calcineurin Inhibitors

Non-steroidal anti-inflammatory alternatives to corticosteroids.

Indications:

• Facial dermatitis (avoid steroid atrophy)
• Chronic dermatitis requiring long-term therapy
• Steroid-refractory dermatitis

Advantages: No skin atrophy, safe for long-term use on face

Disadvantages: Burning/stinging on application (especially if applied to inflamed skin), less effective than moderate-potent corticosteroids, more expensive

Black box warning: Theoretical increased lymphoma risk (not confirmed in humans); avoid in children less than 2 years

Antihistamines

Antihistamines provide symptomatic relief of pruritus but do not treat the underlying inflammation.

Efficacy: Modest benefit for itch; sedating antihistamines may help via sedative effect rather than antihistamine effect (since histamine is not primary mediator in ACD)

Soothing/Supportive Measures

Antibiotics (for Secondary Infection)

Clinical Pearls:

• Honey-colored crusting → impetiginization (Staphylococcus aureus or Streptococcus)
• Increasing pain, warmth, spreading erythema, fever → cellulitis
• MRSA consideration in recurrent infections, healthcare workers, injection drug users

Emerging/Alternative Therapies

---

Disposition

Discharge Criteria (Outpatient Management)

Most patients with contact dermatitis can be managed in outpatient setting:

• Diagnosis established
• Appropriate topical or systemic therapy prescribed
• Allergen/irritant avoidance counseling provided
• Adequate analgesia/antipruritic therapy
• Follow-up arranged (2-4 weeks or sooner if not improving)
• Return precautions reviewed

Follow-Up:

• Reassess in 2-4 weeks
• If not improving: reconsider diagnosis, assess compliance, consider patch testing
• If recurrent: patch testing indicated
• Occupational cases: may require Workers' Compensation evaluation, job modification

Admission Criteria (Rare)

• Severe bullous reaction with extensive skin barrier loss, fluid/electrolyte imbalance, risk of infection
• Erythroderma (> 90% BSA)
• Airway compromise (severe facial/oropharyngeal edema from hair dye or other severe ACD)
• Severe cellulitis requiring IV antibiotics
• Unable to care for self at home
• Failed outpatient management with severe symptoms

Referral

---

Patient Education

Condition Explanation

"Contact dermatitis is a skin rash caused by direct contact with a substance that either irritates your skin or triggers an allergic reaction. There are two main types:

1. Irritant contact dermatitis: Your skin is directly damaged by a harsh substance like soap, detergent, or chemicals. This is more common.

2. Allergic contact dermatitis: Your immune system reacts to a substance you're allergic to, like nickel in jewelry, fragrances in cosmetics, or poison ivy. The rash usually appears 1-3 days after contact.

The key to treatment is identifying what caused the rash and avoiding it. Medications like steroid creams or pills help reduce inflammation and itch while your skin heals."

Avoidance Strategies

General:

• Identify and avoid the substance that caused the rash
• Read product labels carefully
• Choose fragrance-free, hypoallergenic products when possible
• Wear protective gloves when handling potential irritants
• Apply barrier creams before exposure if avoidance impossible

Specific Allergens:

Nickel:

• Avoid costume jewelry; use hypoallergenic metals (titanium, surgical stainless steel, gold > 18K, platinum)
• Cover metal buttons, belt buckles, zippers with cloth or coat with clear nail polish
• Avoid handling coins, keys for prolonged periods
• Dietary nickel restriction may help systemically absorbed nickel allergy (controversial)

Fragrances:

• Use fragrance-free (not just "unscented") products
• Avoid perfumes, scented lotions, air fresheners
• Check ingredient lists: "fragrance," "parfum," "essential oils"

Preservatives (MI/MCI):

• Read product labels
• Avoid products containing methylisothiazolinone, methylchloroisothiazolinone
• Choose preservative-free alternatives

Poison Ivy/Oak/Sumac:

• Learn to identify plants: "Leaves of three, let it be"
• Wear long sleeves, pants, gloves when hiking/gardening in areas with these plants
• If exposed: wash skin with soap and water immediately (within 10-15 minutes)
• Wash clothing and tools that may have contacted plant
• Urushiol can remain on pet fur, garden tools—wash these as well

Rubber (gloves):

• If allergic to rubber accelerators: use vinyl or nitrile gloves
• If latex allergy (Type I): use non-latex gloves

Occupational:

• Discuss exposures with employer
• Use protective equipment (gloves, aprons)
• Improve ventilation, industrial hygiene
• Consider job modification if severe

Skin Care Recommendations

• Moisturize: Apply fragrance-free, dye-free moisturizer liberally at least twice daily and after hand washing
• Gentle cleansers: Use mild, soap-free cleansers (Cetaphil, CeraVe)
• Avoid hot water: Use lukewarm water; hot water worsens dryness and inflammation
• Pat dry: Gently pat skin dry; avoid vigorous rubbing
• Short showers: Limit bathing time to 5-10 minutes
• Protect hands: Wear gloves when washing dishes, cleaning (use vinyl/nitrile if rubber allergy)

Medication Instructions

Topical Corticosteroids:

• Apply a thin layer to affected areas twice daily (or as prescribed)
• Gently rub in until absorbed
• Avoid face unless specifically prescribed low-potency steroid
• Do not use on open sores or infected skin
• Taper as instructed (do not stop abruptly if using potent steroids)

Systemic Corticosteroids (Prednisone):

• Take with food to reduce stomach upset
• Complete the full course even if symptoms improve (prevents rebound)
• Do not stop early—rebound dermatitis can occur
• Side effects: Increased appetite, mood changes, trouble sleeping, elevated blood sugar
• Notify provider if signs of infection develop

Warning Signs to Return

Seek medical attention if:

• No improvement after 1-2 weeks of treatment
• Worsening despite treatment
• Fever (temperature > 100.4°F/38°C)
• Increasing pain, warmth, redness (suggests infection)
• Pus or honey-colored crusting (suggests infection)
• Spreading rash to new areas
• Facial or throat swelling (especially if difficulty breathing—call 911)
• Signs of systemic illness (fever, chills, malaise)

---

Special Populations

Children

• Contact dermatitis less common in young infants (limited exposure), increases with age
• Nickel allergy common in adolescent females (ear piercing)
• Topical antibiotics (neomycin), fragrances, preservatives, rubber also common
• Treatment: Same principles as adults
  • Use low-potency steroids on face, diaper area
  • Avoid super-high potency steroids
  • "Systemic steroids if severe (weight-based dosing: 1 mg/kg/day prednisone)"
• Patch testing can be performed (same as adults) [21]

Occupational Contact Dermatitis

• Definition: Contact dermatitis caused or exacerbated by workplace exposures

• Epidemiology: Most common occupational skin disease (40-50% of occupational diseases)

• High-risk occupations:

  • Healthcare workers (gloves, disinfectants, medications)
  • Hairdressers (hair dye [PPD], bleach, shampoos)
  • Construction workers (chromate in cement, resins)
  • Food handlers (wet work, food allergens)
  • Metalworkers (cutting fluids, metal allergens)
  • Cleaners (detergents, disinfectants)
  • Mechanics (oils, greases, rubber)

• Diagnosis: Often mixed ICD and ACD; patch testing essential

• Management:

  • Identify workplace exposures
  • Protective equipment (gloves—but gloves themselves can cause rubber ACD)
  • Industrial hygiene measures
  • Job modification or retraining if severe
  • Workers' Compensation evaluation
  • Barrier creams (limited efficacy; not substitute for gloves)

• Prognosis: Often chronic; early intervention improves outcome; poor prognosis if continue in same occupation without modification [5]

Pregnancy

• Safety of Topical Corticosteroids:
  • "Low-medium potency topical steroids: Safe (Category C)"
  • "Super-high potency or prolonged use over large areas: Avoid (theoretical HPA axis suppression)"
  • Use lowest potency for shortest duration
• Systemic Corticosteroids:
  • "Prednisone: Category C"
  • Use if benefits outweigh risks (severe widespread dermatitis, facial involvement)
  • Short courses generally considered safe
  • Avoid first trimester if possible (theoretical increased cleft palate risk—controversial)
• Antihistamines:
  • "First-generation (diphenhydramine, chlorpheniramine): Category B—safe"
  • "Second-generation (cetirizine, loratadine): Category B—safe"
• Patch testing: Generally avoided during pregnancy (theoretical risk of active sensitization); defer to postpartum unless essential

Elderly

• Increased risk of irritant contact dermatitis due to:
  • Impaired barrier function (decreased lipids, slower barrier repair)
  • Decreased immune function
  • Multiple medications (polypharmacy)
• Stasis dermatitis common on lower legs (often misdiagnosed as contact dermatitis)
• Contact allergy to topical medications (neomycin, corticosteroids, preservatives in creams)
• Treatment considerations:
  • Avoid super-high potency steroids (skin atrophy, fragility)
  • Emphasize barrier repair (emollients)
  • Review all topical medications (potential allergens)

Chronic Hand Eczema

• Most common and debilitating form of contact dermatitis
• Affects 10% of population at some point
• High impact on quality of life and occupational disability
• Often multifactorial: ICD + ACD + atopic predisposition
• Clinical patterns:
  • Hyperkeratotic (palmar)
  • Vesicular/pompholyx (sides of fingers, palms)
  • Fingertip dermatitis
  • Fissured
• Evaluation: Patch testing essential (identifies allergen in 20-50%)
• Treatment:
  • Identify and avoid allergens/irritants
  • "Strict hand care regimen: gentle cleansers, frequent emollients, cotton gloves under vinyl gloves"
  • High-potency topical steroids (ointments)
  • "Systemic therapy if severe: prednisone burst, phototherapy, alitretinoin (Europe), dupilumab [20]"
• Prognosis: Chronic, relapsing; good compliance with avoidance and hand care improves prognosis [22]

---

Quality Metrics

Performance Indicators

Documentation Requirements

• Suspected trigger: Document exposure history
• Distribution and morphology: Body site(s), acute vs. chronic features
• Vesiculation: Presence suggests ACD
• Secondary infection: Honey crusting, purulence
• Treatment plan: Specific medications, potency of steroids, duration
• Avoidance counseling: Documented discussion
• Follow-up plan: When and under what circumstances to return
• Occupational: If work-related, document for Workers' Compensation

---

Key Clinical Pearls

Diagnostic Pearls

• Pruritus is the hallmark: Intense itch differentiates from cellulitis (pain/tenderness)
• Linear streaks = plant contact: Classic for poison ivy/oak/sumac (urushiol)
• Geometric/well-demarcated = external cause: Sharp borders suggest contactant
• "Dimple sign": Dermatitis precisely at site of metal contact (nickel under watch, belt buckle)
• Eyelid dermatitis often from hands: Nail polish transferred to eyelids by rubbing eyes
• Delayed onset (24-72 hrs) = ACD: Immediate onset = ICD
• Patch testing is gold standard: For identifying allergens in ACD; requires 2 weeks off systemic steroids
• ICD accounts for 80%: But ACD is more memorable and requires patch testing
• Occupational clue: Improves on weekends/vacations, worsens at work
• Spares certain areas: Interdigital web spaces often spared in nickel dermatitis (no contact)
• Cross-reactivity common: Nickel + cobalt + chromate; fragrances + Balsam of Peru
• "Angry back" syndrome: Generalized patch test reactivity from testing during flare

Treatment Pearls

• Wash immediately after plant exposure: Removes urushiol if within 10-15 minutes (soap and water)
• Topical steroids: potency matters: Match potency to site (low for face, high for palms/soles)
• Ointments > creams for chronic: Ointments more occlusive, better for dry/lichenified skin
• Systemic steroids: 2-3 week taper required: Short courses (less than 10-14 days) cause rebound dermatitis
• Methylprednisolone dose pack not recommended: Insufficient duration for contact dermatitis
• Antihistamines help itch but don't treat inflammation: Modest benefit; sedating types may help via sedation
• Emollients are cornerstone: Barrier repair; apply liberally and frequently
• Treat secondary infection: Honey crusts = impetiginization; add antibiotics
• Calcineurin inhibitors for face: Avoid steroid atrophy; tacrolimus/pimecrolimus
• Steroid allergy is real: Paradoxical worsening on topical steroid → patch test to corticosteroid

Disposition Pearls

• Most discharged with topical ± systemic therapy: Outpatient management
• Refer for patch testing: Chronic, recurrent, occupational, uncertain diagnosis
• Educate on avoidance: Critical for long-term success
• Return precautions: Fever, spreading redness/warmth (infection), no improvement in 1-2 weeks
• Occupational cases: Workers' Comp, job modification, industrial hygiene consult
• Admission rare: Severe bullous, erythroderma, airway compromise, severe cellulitis

Prevention Pearls

• Barrier protection: Gloves (but beware rubber ACD), barrier creams (limited efficacy)
• Emollients: Prevent barrier dysfunction; apply before and after exposure
• Avoid irritants: Harsh soaps, hot water, excessive hand washing
• Product selection: Fragrance-free, hypoallergenic, preservative-free when possible
• Occupational hygiene: Ventilation, protective equipment, reduce exposure time
• Early intervention: Treat early dermatitis promptly to prevent chronicity

---

References

1. Fonacier L, Noor I. Contact dermatitis and patch testing for the allergist. Ann Allergy Asthma Immunol. 2018;120(6):592-598. doi:10.1016/j.anai.2018.02.010

2. Brites GS, Ferreira I, Sebastião AI, et al. Allergic contact dermatitis: From pathophysiology to development of new preventive strategies. Pharmacol Res. 2020;162:105282. doi:10.1016/j.phrs.2020.105282

3. Fonacier L, Uter W, Johansen JD. Recognizing and Managing Allergic Contact Dermatitis: Focus on Major Allergens. J Allergy Clin Immunol Pract. 2024;12(6):1406-1418. doi:10.1016/j.jaip.2024.03.033

4. Thyssen JP, Linneberg A, Menné T, Johansen JD. The epidemiology of contact allergy in the general population—prevalence and main findings. Contact Dermatitis. 2007;57(5):287-299. doi:10.1111/j.1600-0536.2007.01220.x

5. Jakasa I, Thyssen JP, Kezic S. The role of skin barrier in occupational contact dermatitis. Exp Dermatol. 2018;27(8):909-914. doi:10.1111/exd.13704

6. Esser PR, Martin SF. Pathomechanisms of Contact Sensitization. Curr Allergy Asthma Rep. 2017;17(12):83. doi:10.1007/s11882-017-0752-8

7. Engebretsen KA, Thyssen JP. Skin Barrier Function and Allergens. Curr Probl Dermatol. 2016;49:90-102. doi:10.1159/000441550

8. Irvine AD, McLean WH, Leung DY. Filaggrin mutations associated with skin and allergic diseases. N Engl J Med. 2011;365(14):1315-1327. doi:10.1056/NEJMra1011040

9. Saint-Mezard P, Berard F, Dubois B, Kaiserlian D, Nicolas JF. The role of CD4+ and CD8+ T cells in contact hypersensitivity and allergic contact dermatitis. Eur J Dermatol. 2004;14(3):131-138. PMID: 15246935

10. Vocanson M, Hennino A, Chavagnac C, et al. Contribution of CD4(+) and CD8(+) T-cells in contact hypersensitivity and allergic contact dermatitis. Expert Rev Clin Immunol. 2005;1(1):75-86. doi:10.1586/1744666X.1.1.75

11. Girolomoni G, Gisondi P, Ottaviani C, Cavani A. Immunoregulation of allergic contact dermatitis. J Dermatol. 2004;31(4):264-270. doi:10.1111/j.1346-8138.2004.tb00663.x

12. Lefevre MA, Vocanson M, Nosbaum A. Role of tissue-resident memory T cells in the pathophysiology of allergic contact dermatitis. Curr Opin Allergy Clin Immunol. 2021;21(4):326-333. doi:10.1097/ACI.0000000000000756

13. Albanesi C. Keratinocytes in allergic skin diseases. Curr Opin Allergy Clin Immunol. 2010;10(5):452-456. doi:10.1097/ACI.0b013e32833e08ae

14. Jakasa I, Thyssen JP, Kezic S. The role of skin barrier in occupational contact dermatitis. Exp Dermatol. 2018;27(8):909-914. doi:10.1111/exd.13704

15. Mowad CM, Anderson B, Scheinman P, et al. Allergic contact dermatitis: Patient diagnosis and evaluation. J Am Acad Dermatol. 2016;74(6):1029-1040. doi:10.1016/j.jaad.2015.02.1139

16. Fonacier L, Bernstein DI, Pacheco K, et al. Contact dermatitis: A practice parameter—Third update. J Allergy Clin Immunol Pract. 2015;3(3 Suppl):S1-S39. doi:10.1016/j.jaip.2015.02.009

17. Usatine RP, Riojas M. Diagnosis and Management of Contact Dermatitis. Am Fam Physician. 2010;82(3):249-255. PMID: 20672788

18. Gladman AC. Toxicodendron dermatitis: Poison ivy, oak, and sumac. Wilderness Environ Med. 2006;17(2):120-128. doi:10.1580/PR31-05.1

19. Schram ME, Roekevisch E, Leeflang MM, et al. A randomized trial of methotrexate versus azathioprine for severe atopic eczema. J Allergy Clin Immunol. 2011;128(2):353-359. doi:10.1016/j.jaci.2011.03.024

20. Worm M, Bauer A, Elsner P, et al. Efficacy and safety of topical delgocitinib in patients with chronic hand eczema: data from a randomized, double-blind, vehicle-controlled phase IIa study. Br J Dermatol. 2020;182(5):1103-1110. doi:10.1111/bjd.18469

21. Zug KA, McGinley-Smith D, Warshaw EM, et al. Contact allergy in children referred for patch testing: North American Contact Dermatitis Group data, 2001-2004. Arch Dermatol. 2008;144(10):1329-1336. doi:10.1001/archderm.144.10.1329

22. Agner T, Elsner P. Hand eczema: epidemiology, prognosis and prevention. J Eur Acad Dermatol Venereol. 2020;34 Suppl 1:4-12. doi:10.1111/jdv.16061